The long range goals of the studies described in this application are to elucidate how acute exposure to intermittent hypoxia-reoxygenation influences signaling mechanisms that control coronary and pulmonary vascular function. This laboratory has elucidated many aspects of how reactive oxygen species (ROS) and nitric oxide-derived species (RNS) interact with signaling systems which regulate processes that control vascular contraction and relaxation, and tissue respiratory processes, with an emphasis on how these mechanisms could function in responses elicited by changes in oxygen tension. It is hypothesized that ROS and RNS have important roles in the early modifications of vascular function caused by acute exposure to intermittent hypoxia. Thus, the overall goals of this project are to elucidate the roles of ROS and RNS in the initial alterations of vascular signaling mechanisms caused by exposure to intermittent hypoxia-reoxygenation that control the function of bovine coronary and pulmonary arteries. The first aim focuses on determining how intermittent hypoxia-reoxygenation alters signaling mechanisms that control bovine coronary and pulmonary arterial smooth muscle contractile function. The second aim examines how intermittent hypoxia-reoxygenation alters endothelium-derived signaling mechanisms that regulate coronary and pulmonary arterial function in large vessel and microvascular preparations. The third aim studies how intermittent hypoxia-reoxygenation alters oxygen sensing signaling mechanisms that regulate coronary and pulmonary arterial function. These studies could provide fundamental information on how intermittent hypoxia contributes to the initial alterations in vascular function which could be important factors in the pathogenesis of vascular diseases associated with sleep apnea and related disorders.